It has been recently demonstrated that an increase in perfusate calcium concentration within the millimolar range results in an increase in "resting" force in unstimulated rat cardiac muscle. To determine whether this apparent calcium influx occurs via a passive "leak" of calcium down its electrochemical gradient or might be mediated, in part at least, via a Na/Ca exchange was the focus of the present study. In isometric rat right ventricular papillary muscles equilibrated at 29 C, stimulation was stopped and sodium, potassium or calcium concentrations were varied in various combinations in the presence and absence of ouabain and caffeine. The resulting apparent change in cellular calcium was monitored by measurements of resting force. The apparent increase in cellular calcium following a step increase in perfusate calcium was highly dependent on conditions that effect intracellular sodium, the results are best explained by a sarcolemmal Na/Ca exchange mechanism. Furthermore, the results suggest that this mechanism can operate in the direction to load the cell with calcium even in the unstimulated state and in part modulates the calcium-dependent portion of resting force observed in the rat.